Chronic obstructive pulmonary disease (COPD) is the fourth leading cause of death in the world population. In addition to airflow obstruction, COPD is associated with multiple systemic manifestations, including impaired nutritional status or malnutrition and changes in body composition (low muscle mass, LMM). Poor nutritional status and sarcopenia in subjects with COPD leads to a worse prognosis and increases health-related costs. Data from previous studies indicate that 30-60% of subjects with COPD are malnourished, 20-40% have low muscle mass, and 15-21.6% have sarcopenia. This study aimed to assess the prevalence of malnutrition, sarcopenia, and malnutrition-sarcopenia syndrome in elderly subjects with COPD and investigate the relationship between COPD severity and these conditions.

Sarcopenia is defined as the disease of muscle loss and dysfunction. The prevalence of sarcopenia is strongly age-dependent. It could bring about disability, hospitalization, and mortality. The purpose of this study was to identify plasma metabolites associated with possible sarcopenia and muscle function to improve disease monitoring and understand the mechanism of muscle strength and function decline.

Sarcopenia is defined as the loss of muscle mass and strength. Despite the seriousness of this disease, a single diagnostic criterion has not yet been established. Few studies have reported the prevalence of sarcopenia globally, and there is a high level of heterogeneity between studies, stemmed from the diagnostic criteria of sarcopenia and the target population. The aims of this systematic review and meta-analysis were (i) to identify and summarize the diagnostic criteria used to define sarcopenia and severe sarcopenia and (ii) to estimate the global and region-specific prevalence of sarcopenia and severe sarcopenia by sociodemographic factors.

Sarcopenia is the age-related loss of muscle mass, strength, and function. Epigenetic processes such as DNA methylation, which integrate both genetic and environmental exposures, have been suggested to contribute to the development of sarcopenia. This study aimed to determine whether differences in the muscle methylome are associated with sarcopenia and its component measures: grip strength, appendicular lean mass index (ALMi), and gait speed.

Although handgrip strength (HGS) asymmetry has clinical screening utility, its relevance to sarcopenia is unknown. This study examined the relationship between HGS asymmetry and sarcopenia signatures, and explored the relevance of circulating neural/neuromuscular markers.

This study aimed to (1) determine the intraobserver and interobserver reliability of ultrasonographic measurement of muscle thickness (MT) and cross-sectional area (CSA) of the rectus femoris and biceps brachii, correlating these values with manual measurements on dissected cadavers and (2) develop the first semiquantitative musculoskeletal ultrasound (MSUS) scoring system of muscle morphology in sarcopenia and assess its intraobserver and interobserver reliability. In addition, the MSUS morphology score was compared with the corresponding histological images to verify concurrent validity.

Several studies have examined gut microbiota and sarcopenia using 16S ribosomal RNA amplicon sequencing; however, this technique may not be able to identify altered specific species and functional capacities of the microbes. We performed shotgun metagenomic sequencing to compare the gut microbiome composition and function between individuals with and without sarcopenia.

Early prevention of sarcopenia is a recommendation to reduce morbidity, mortality and improve quality of life. Several non-pharmacological interventions to reduce the risk of sarcopenia in community-dwelling older people have been proposed. Therefore, there is a need to identify the scope and differences of these interventions. This scoping review will summarise the nature and extent of the existing literature that describes and examines non-pharmacological interventions for community-dwelling older adults with possible sarcopenia or sarcopenia.

Sarcopenia, which is characterized by the loss of skeletal muscle, has been reported to contribute to development of physical disabilities, various illnesses, and increasing mortality. MicroRNAs (miRNAs) are small non-coding RNAs that inhibit translation of target messenger RNAs. Previous studies have shown that miRNAs play pivotal roles in the development of sarcopenia. Therefore, this systematic review focuses on miRNAs that regulate sarcopenia.

Comprehensive geriatric assessment (CGA) is a multidimensional diagnostic process enabling evaluation of elderly patients' physical and mental health status that implies implementation of the management targeted on the preservation of functional independence. Sarcopenia is a common but often underdiagnosed geriatric syndrome associated with increased likelihood of functional dependence and mortality risk. The main objectives of the study were the evaluation of sarcopenia prevalence in the patient group subjected to CGA with the upgraded EWGSOP2 algorithm considering muscle strength as the key criterion and usage of bioimpedance (BIA) muscle mass assessment. The study group consisted of 101 patients (76 women and 25 men) admitted for planned CGA to the Geriatrics Department of Wroclaw University Hospital. A diagnosis of sarcopenia was made according to the EWGSOP2 protocol. Body composition was determined with the bioimpedance technique. Functional status was assessed with ADLs from the VES-13 scale and additional questions. Sarcopenia was diagnosed in 16.8% of the study participants. Sarcopenic individuals presented worse functional status and impaired social activity. Muscle strength, gait speed and muscle mass below cut-off values were associated with dependence found in ADLs. Results showed that sarcopenia is a common impairment correlated with worse functional status and vulnerability to adverse outcomes. BIA can be treated as an accessible and accurate technique for muscle mass measurement in screening for sarcopenia, and the EWGSOP2 algorithm should be an essential part of the routine CGA procedure.

Sarcopenia, defined as muscle weakness and fiber atrophy, of respiratory muscles such as the diaphragm (DIAm) has not been well characterized. The DIAm is the main inspiratory muscle and knowledge of DIAm sarcopenia is important for establishing the effects of aging on respiratory function. We hypothesized that aging is associated with a loss of DIAm force and reduced fiber cross-sectional area (CSA), and that these changes vary across fiber types. DIAm sarcopenia was assessed in young (5 month; n = 11) and old (23 month; n = 12) wild-type mice reflecting ~100 and 75% survival, respectively. In addition, DIAm sarcopenia was evaluated in BubR1(H/H) mice (n = 4) that display accelerated aging (~60% survival at 5 months) as a result of expression of a hypomorphic allele (H) of the mitotic checkpoint protein BubR1. Maximum specific force (normalized for CSA) of the DIAm was 34% less in old mice and 57% lower in BubR1(H/H) mice compared to young mice. Mean CSA of type IIx and/or IIb DIAm fibers was 27% smaller in old wild-type mice and 47% smaller in BubR1(H/H) mice compared to young mice. Mean CSA of type I or IIa fibers was not different between groups. Collectively these results demonstrate sarcopenia of the DIAm in aging wild-type mice and in BubR1(H/H) mice displaying accelerated aging. Sarcopenia may limit the ability of the DIAm to accomplish expulsive, non-ventilatory behaviors essential for airway clearance. As a result, these changes in the DIAm may contribute to respiratory complications with aging.

Regular physical activity (PA) is associated with reduced risk of the development and progression of musculoskeletal, metabolic and vascular disease. However, PA declines with age and this can contribute to multiple adverse outcomes. The aims of this study were to describe the relationship between accelerometer-determined PA, body composition and sarcopenia (the loss of muscle mass and function with age). Seven-day PA was measured using the GENEactiv accelerometer among 32 men and 99 women aged 74-84 years who participated in the Hertfordshire Sarcopenia Study. We measured mean daily acceleration and minutes/day spent in non-sedentary and moderate-to-vigorous physical activity (MVPA) levels. Body composition was measured by dual-energy X-ray absorptiometry, muscle strength by grip dynamometry and function by gait speed. Sarcopenia was defined according to the EWGSOP diagnostic algorithm. Men and women spent a median (inter-quartile range) of 138.8 (82, 217) and 186 (122, 240) minutes/day engaging in non-sedentary activity but only 14.3 (1.8, 30.2) and 9.5 (2.1, 18.6) min in MVPA, respectively. Higher levels of PA were associated with reduced adiposity, faster walking speed and decreased risk of sarcopenia. For example, a standard deviation (SD) increase in mean daily acceleration was associated with an increase in walking speed of 0.25 (95% CI 0.05, 0.45) SDs and a reduction in the risk of sarcopenia of 35% (95% CI 1, 57%) in fully adjusted analyses. PA was not associated with hand grip strength. Community-dwelling older adults in this study were largely sedentary but there was evidence that higher levels of activity were associated with reduced adiposity and improved function. PA at all intensity levels in later life may help maintain physical function and protect against sarcopenia.

The diversity between the muscle cellular interactome of dependent and independent elderly people is based on the interrelationships established between different cellular mechanisms, and alteration of this balance modulates cellular activity in muscle tissue with important functional implications.

Sarcopenia is increasingly recognized as a correlate of ageing and is associated with increased likelihood of adverse outcomes including falls, fractures, frailty and mortality. Several tools have been recommended to assess muscle mass, muscle strength and physical performance in clinical trials. Whilst these tools have proven to be accurate and reliable in investigational settings, many are not easily applied to daily practice.

Sarcopenia is intricately related to aging associated diseases, such as neuropsychiatric disorders, oral status, and chronic diseases. Dementia and depression are interconnected and also related to sarcopenia. The preliminary shift from robust to sarcopenia (i.e., pre-sarcopenia) is an important albeit underdiscussed stage and is the focus of this study. Identifying factors associated with pre-sarcopenia may lead to sarcopenia prevention. To separately examine the effects of dementia and depression on pre-sarcopenia/sarcopenia, we conducted multiple analyses. This cross-sectional study used health checkup data from a rural Japanese island. The participants were aged 60 years and above, and the data included muscle mass, gait speed, handgrip strength, oral status (teeth and denture), chronic diseases (e.g., hypertension), dementia (cognitive assessment for dementia, iPad Version), and depression (self-rating depression scale). A total of 753 older adult participants were divided into the sarcopenia (n = 30), pre-sarcopenia (n = 125), and robust (n = 598) groups. An ordered logit regression analysis indicated that age and depression were positively correlated with sarcopenia, while hypertension was negatively associated with it. A multiple logistic regression analysis between the robust and pre-sarcopenia groups showed significant associations between the same three variables. Depression was associated with pre-sarcopenia, but not dementia. There was also a significant association between hypertension and pre-sarcopenia. Further research is needed to reveal whether the management of these factors can prevent sarcopenia.

to examine the clinical evidence reporting the prevalence of sarcopenia and the effect of nutrition and exercise interventions from studies using the consensus definition of sarcopenia proposed by the European Working Group on Sarcopenia in Older People (EWGSOP).

The human skeletal muscle has a pivotal role in preserving health by maintaining mobility, balance, and metabolic homeostasis. Significant muscle loss as a part of aging and accelerated by disease leads to sarcopenia which becomes an important predictor of quality of life in older persons. Therefore, clinical screening for sarcopenia and validation by precise qualitative and quantitative measurement of skeletal muscle mass (MM) and function is at the center-stage of translational research. Many imaging modalities are available, each having their strengths and limitations, either in interpretation, technical processes, time constraints, or expense. B-mode ultrasonography (US) is a relatively novel approach to evaluating muscle. It can measure several parameters such as MM and architecture simultaneously including muscle thickness, cross-sectional area, echogenicity, pennate angle, and fascicle length. It can also evaluate dynamic parameters like muscle contraction force and muscle microcirculation. US has not gained global attention due to a lack of consensus on standardization and diagnostic threshold values to diagnose sarcopenia. However, it is an inexpensive and widely available technique with clinical applicability. The ultrasound-derived parameters correlate well with strength and functional capacity and provide potential prognostic information. Our aim is to present an update on the evidence-based role of this promising technique in sarcopenia, its advantages over the existing modalities, and its limitations in actual practice with the hope that it may emerge as the "stethoscope" for community diagnosis of sarcopenia.

Sarcopenia seriously affects the quality of life of the elderly, but its molecular mechanism is still unclear. Degeneration in muscle innervation is related to age-related movement disorders and muscle atrophy. The expression of CHRNA1 is increased in the skeletal muscle of the elderly, and in aging rodents. Therefore, we investigated whether CHRNA1 induces the occurrence and development of sarcopenia. Compared with the control group, local injection of AAV9-CHRNA1 into the hindlimb muscles decreased the percentage of muscle innervation. At the same time, the skeletal muscle mass decreased, as manifested by a decrease in the gastrocnemius mass index and the cross-sectional area of the muscle fibers. The function of skeletal muscle also decreased, which was manifested by decreases of compound muscle action potential and muscle contractility. Therefore, we concluded that upregulation of CHRNA1 can induce and aggravate sarcopenia.

The world is facing the new challenges of an aging population, and understanding the process of aging has therefore become one of the most important global concerns. Sarcopenia is a condition which is defined by the gradual loss of skeletal muscle mass and function with age. In research and clinical practice, sarcopenia is recognized as a component of geriatric disease and is a current target for drug development. In this review we define this condition and provide an overview of current therapeutic approaches. We further highlight recent findings that describe key pathophysiological phenotypes of this condition, including alterations in muscle fiber types, mitochondrial function, nicotinamide adenine dinucleotide (NAD+) metabolism, myokines, and gut microbiota, in aged muscle compared to young muscle or healthy aged muscle. The last part of this review examines new therapeutic avenues for promising treatment targets. There is still no accepted therapy for sarcopenia in humans. Here we provide a brief review of the current state of research derived from various mouse models or human samples that provide novel routes for the development of effective therapeutics to maintain muscle health during aging.

Reactive oxygen species (ROS) accumulation is a cardinal feature of skeletal muscle atrophy. ROS refers to a collection of radical molecules whose cellular signals are vast, and it is unclear which downstream consequences of ROS are responsible for the loss of muscle mass and strength. Here, we show that lipid hydroperoxides (LOOH) are increased with age and disuse, and the accumulation of LOOH by deletion of glutathione peroxidase 4 (GPx4) is sufficient to augment muscle atrophy. LOOH promoted atrophy in a lysosomal-dependent, proteasomal-independent manner. In young and old mice, genetic and pharmacological neutralization of LOOH or their secondary reactive lipid aldehydes robustly prevented muscle atrophy and weakness, indicating that LOOH-derived carbonyl stress mediates age- and disuse-induced muscle dysfunction. Our findings provide novel insights for the role of LOOH in sarcopenia including a therapeutic implication by pharmacological suppression.